The document presents findings on the A20 gene, which encodes a zinc finger protein that inhibits NF-kB activity and TNF-induced apoptosis. The study found that C57 and FVB mouse strains have a coding difference in A20 that generates a phosphorylation site in C57 mice. C57-A20 was less effective at shutting down TNF-induced NF-kB activity and C57 cells were less susceptible to TNF-induced apoptosis compared to FVB cells. This suggests less active A20 in C57 mice leads to increased inflammation and reduced apoptosis, while more active A20 in FVB mice decreases inflammation and increases apoptosis, contributing to differences in atherosclerosis susceptibility between the strains.